FOLR2 and idiopathic pulmonary fibrosis: Because human IPF lungs are also comprised predominantly of FRβ+ M2‐polarized macrophages that are thought to contribute most prominently to development of fibrosis (Prasse et al, 2006; Braga et al, 2015; Byrne et al, 2015), these data suggest that FA‐TLR7‐54 might similarly reprogram human IPF macrophages to a less profibrotic phenotype.